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MANIFFESTATIONS of ARF
DEFINITION
No consensus Multiple Relative rise in Serum Creatinine > 0.5mg/dl if baseline creatinine is normal > 1 mg/dl if baseline serum creatinine is high
Lack of sensitivity of BUN and creatinine Need for Biomarkers Kidney Injury Molecules-1(KIM-1) increased in Patients with Acute Tubular Necrosis None available for cliniical utility yet
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Epidemiology of ARF
Incidence, etiology and outcome varied depending on Population studied and Definition used Mostly in-Patient than out Patient 5-7% of hospital admissions Mortality varies between 20%-85% depending on cause
ARF Classification
Prerenal ARF
Hemodynamically mediated reduction in GFR in absence on Renal Parenchymal injury. ARF resolves if hemodynamic insult is reversed If hemodynamic insult is sustained, can result in overt renal injury
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Renal ARF
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Postrenal ARF
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Prerenal Azotemia
Prerenal Azotemia
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Renal Autoregulation
Efferent vasoconstriction
Angiotension 11
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Prerenal Azotemia
ACEI & ARB have greatest benefits in Patients with high risk of ARF
Old age Diabetics Cardiomyopathy CHF with higher dose oh Diuretic Renal Vascular disease Chronic Kidney disease
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Efferent Vasodilatation deceases GFRmedications Lower GFR raises serum creatinie but usually less than 30% Must monitor serum creatinine and electrolytes before and after starting or changing dose of these medications Stop if ARF Correct volume status W/u for renal Artery Stenosios Can reintroduce cautiously if reversible factors corrected
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Both COX1/Cox!! Inhibitors cause lower Prostaglandins synthesis Impairs Afferent vasodilatation decrease Glomerular perfusion Effect greatest in high risk population
Respiratory compromise Decreased cardiac output Intestinal ischemia Hepatic Dysfunction Oliguric ARF
Post-Renal ARF
Obstruction complete or Partial Anuria or variable urine output Recovery depends on duration of obstruction Conditions Sonogram may not show obstruction,
ARF- Renal
Glomerulus- Acute Glomerulonephritis Tubules- Acute Tubular Necrosis Interstitium- Acute Interstial Nephritis Vascular- Atheroembolism
Ischemic vs Nephrotoxic Most frequently multi-factorial Medical vs Surgical Ischemic- Hypotension,shock Nephrotoxic- Dye induced, Rhabdomyolysis
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Initiation, maintenance, recovery Phases Mortality from very low to very high Potentially Preventable Long term outcome in survivors very good
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Radiocontrast Nephropathy
10% of Hospital acquired ATN Mild and Transient in Majority Risk factors,
Amount of Dye(> 100cc) Volume Depletion Renal Insufficiency DM Old Age CHF ACEI or NSAIDs
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Radiocontrast Nephropathy
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Radiocontrast Nephropathy
Pathogenesis incompletely understood Severe Renal vasoconstriction within seconds of contrast administration Direct Renal Tubular injury FENa < 1%
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Radiocontrast Nephropathy
Independent risk factor of death Prevention in high risk Patients Consider Alternate imaging.g. MRI Volume repletion with Saline Minimize amount of Dye Low Osmolality contrast media? N-Acetylcysteine(Mucomyst)? Fenoldopam-Selective Dopamine agonist? Lasix, Mannitol, Dopamine not helpful, may be risky Prophylactic Hemodialysis- not helpful 29
Radiocontrast Nephropathy
N-Acetylcysteine reducing agent, scavenge reactive oxygen species(ROS) No good large randomized trial to prove its efficacy Impact on morbidity and mortality unknown Used commonly in practice b/o potential benefits and lack of Toxicity
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Aminoglycoside Nephrotoxicity
Usually after 7-10 days Depends on dose and frequency Direct Proximal Tubular injury Once a day dosing may be less Nephrotoxic K. Ca. MG wasting Risk factors- age, Renal insufficiency, Dose,Volume depletion
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FENa < 1% U/A- Heme/+vie but no RBC Aggressive Volume replacement Urinary Alkalization?, Mannitol?
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Amphotericin B Nephrotoxiciy
Very high incidence of ARF Binds to sterol in cell membrane Multiple sites in Nephrons Distal Tubular Acidosis Mg and K wasting Dose dependent Liposomal Amphotercin formulation less toxic Saline loading helpful
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Postoperative ARF
ARF after vascular,cardiac and major abdominal surgery. Very high mortality Multifactorial 1-5% after CABG. Risk factors,
Renal disease, cardiogenic shock, emergent surgery, Left main disease etc,
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Classical triad(fever rash & eosinophilia) not usually seen Mostly Drug related e.g. Cipro Infection : Strept., Staph, CMV, EB virus, Hantaan virus etc Systemic Diseases : SLE, Sarcoidosis. Eosinophiluria may be absent Dx by renal Biopsy. Rx supportive, Hold Drug, Steroids ?
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Atheroembolic ARF
Require high degree of suspicion Cholesterol emboli Renal failure acute or subacute Multisystem disorder Lived reticularis Digital Ischemia(Blue Toe Syndrome) GI bleed, TIA, Rahbdomyolysis
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Atheroembolic ARF
ARF after vascular procedure ARF can be abrupt needing dialysis within few days. Can be subacute occurring in staggered steps separated by stable renal function. Patients on Anticoagulants are at high risk Eosinphilia, eosinphiluria, low complement. High mortality
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Hepatorenal Syndrome
Profound renal vasoconstriction Resemble Pre-renal Azotemia Volume Expansion fail to improve renal function. Pathogenesis incompletely understood Oligiuric ARF, FENa low Diagnosis of exclusion
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Hepatorenal Syndrome
Two Types Type 1 HRS: rapid ARF, hospitalized Pt.,>90% mortality Type 11 HRS : insidious onset, slow progression of RI, refractory ascites, better prognosis. ATN vs HRS Low FENa I n ATN casts in Bilirubinemia with HRS
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Hepatorenal Syndrome
Rx difficult Volume expansion with Albumin Terlipressin(vasopressin analogue) Midodrine (selective alpha 1 adrenergic agonist)+ octreotide(a somstoastatin analogue) TIPS, Liver Transplantation Dialysis in selective Patients
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ARF in HIV/AIDS
Prerenal Azotemia Renal salt wasting from Adrenal Insufficiency. HIV Nephropathy High risk for ATN Drug side effects e.g. Pentamidine. Crystal nephropathy(indinavir) TTP(prognosis worse ) Rhabomyolysis
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Less common Rapidly Progressive Glomerulonephritis include vasculitis, SLE, Wagner's Active Urinary sediments(RBC cast diagnostic) Higher degree of Proteinuria Serology helpful(ANCA, ANA,IgMantibodyetc0 Renal Biopsy usually required. Early diagnosis essential to prevent ESRD Rx with Steroids and Cytoxan 43
Rx of ARF
No proven Drugs Many cause preventable Volume expansion Withdrawal of Drugs Diuretics help in management but not curative Dopamine potentially harmful
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RRT in ARF
Renal Replacement Therapy usually the only option in severe ARF. Indication of RRT
HYPERKALEMIA METABOLIC Acidosis Uremic Symptoms Fluid Load Prophylactic Intermittent Hemodialysis CVVHD Extended Daily Dialysis(6-12h) Peritoneal Dialysis- not favored
RRT
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CVVHD vs Hemodialysis
HD
more stable Pt, SBP >90, no heparin, allows larger amount of fluid removal in3-4 hours Unstable Pt., low BP with high dose Pressers, allows gradual removal of fluids 24h Allows no heparin dialysis, gradual removal of fluids, but expensive b/o Nursing Support
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CVVHD
EDD
Lot of Questions to answer Frequency of Dialysis Quantification of Dialysis Type of Membrane of Dialysis
Does Erythropoietin improves outcome? Faster fluid removal vs. slow fluid removal?
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